Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Single pharmacological doses of parathyroid hormone, calcitonin, vasopressin, d-aldosterone, or L-triiodothyronine produced a significant increase in the ornithine decarboxylase activity of rat kidney. The activity of kidney ornithine decarboxylase was also enhanced by other hormones, such as pentagastrin and serotonin, which, although they are not known to modify kidney physiology, are secreted by cells having close relationships to the calcitonin-secreting parafollicular cells. The induction of the enzyme was observed in hypophysectomized rats, with or without some other hormone-secreting glands remaining. However, the magnitude of the stimulation elicited by the hormones was somewhat diminished in animals still having the endocrine gland whose hormone was being tested. The maximal stimulation of kidney ornithine decarboxylase activity by parathyroid hormone, calcitonin, vasopressin, L-triiodothyronine, pentagastrin, and serotonin occurred at 4 h after the hormone injection. The enhancement in ornithine decarboxylase activity produced by d-aldosterone was maximal at 3 h after the injection of the hormone. The content of ornithine in the kidney was found to be virtually unchanged whatever the type of hormone treatment. No statistically significant increases in renal ornithine decarboxylase activity of hypophysectomized animals were observed after injection of melatonin or of vitamin D3. Since the stimulating hormones possess clearly different mechanisms of action, the role of cyclic AMP as a general mediator of ornithine decarboxylase induction is questioned.
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PMID:In vivo hormonal induction of ornithine decarboxylase in rat kidney. 18 46

In isolated nerve terminals from ox neurohypophyses the following concentrations of polyamines [pmol (microgram protein)-1 (mean +/- SEM)] were found: spermine: 2.07 +/- 0.14 (n = 3), spermidine: 0.22 +/- 0.01 (n = 4), putrescine: 0.20 +/- 0.01 (n = 4). In secretory granules isolated from the same tissue, the concentrations were: spermine: 0.57 +/- 0.02 (n = 3), spermidine: 0.07 +/- 0.04 (n = 3), putrescine: 0.13 +/- 0.04 (n = 3). After incubation of isolated nerve terminals with the polyamines, they were taken up as a function of time and concentration, approaching saturation at high concentrations. The kinetic parameters of their synthesizing enzyme, ornithine decarboxylase, in ox neurohypophyseal nerve terminals (apparent Km 0.75 mM and Vmax 22.5 pmol mg protein-1 h-1) were comparable to those previously found in cerebral cortex of rats. When isolated, hemilobes from rat neurohypophyses were incubated in a medium which contained spermidine (5 mM), and were stimulated by 56 mM K+, release of vasopressin was smaller than in control experiments. However, after removal of spermidine and after restimulation, 50 min after initial stimulation, the release was significantly elevated. It is suggested that polyamines may take part in modulation of vasopressin release.
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PMID:Polyamines in nerve terminals and secretory granules isolated from neurohypophyses. 144 36

The aim of the present study was to evaluate in vivo the role of polyamines in the secretion of atrial natriuretic peptide (ANP). alpha-Difluoromethylornithine (DFMO) which inhibits ornithine decarboxylase activity and polyamine synthesis was given in drinking water and through intraperitoneal administration to Sprague-Dawley rats. Carotid artery was cannulated for collection of blood samples and measurement of blood pressure following the administration of arginine-vasopressin (AVP). Analysis of polyamines in cardiac tissue indicated that DFMO treatment decreased contents of putrescine and spermidine in cardiac tissue by 80% and 48%, respectively. Quantitation of ANP in plasma by radioimmunoassay indicated that both basal and stimulated levels of ANP in DFMO-treated animals were 21.5% and 50% of those in control rats. The administration of putrescine restored the levels of basal and AVP-stimulated levels of ANP in plasma which confirmed that DFMO effect on ANP secretion occurred specifically through the polyamine pathway.
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PMID:Inhibition of polyamine synthesis impairs the secretion of atrial natriuretic peptide. 153 63

The role of thyroid status in the ontogeny of beta adrenergic receptor control of ornithine decarboxylase (ODC) activity was assessed in hearts and kidneys of neonatal rats. Hyperthyroidism induced by administration of tri-iodothyronine on postnatal days 1 to 5 caused a reduction in the ability of isoproterenol to stimulate cardiac ODC but subsequently accelerated the onset of the postweaning peak of the response; the latter effect was even more prominent when tri-iodothyronine administration was given on postnatal days 14 to 18. Hypothyroidism induced by propylthiouracil administration led to persistent subsensitivity of the cardiac ODC response to beta receptor stimulation. Kidney ODC, which does not become subject to beta receptor regulation until after weaning, was resistant to hyperthyroid-induced changes in reactivity, but hypothyroidism still resulted in long-term response deficits. These results suggest that thyroid hormone is permissive for normal development of the beta receptor-ODC link, and that the euthyroid state provides the optimal conditions for maturation of this signal transduction mechanism. The relative resistance of kidney ODC responses to alterations by hyperthyroidism further indicates that the effects of excess hormone can only be expressed when the receptor-enzyme link is already competent. Finally, thyroid status had equivalent effects on the abilities of vasopressin or angiotensin to stimulate ODC, suggesting that the site of thyroid hormone action is at a transduction locus common to several different receptor types.
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PMID:Role of thyroid hormone in the development of beta adrenergic control of ornithine decarboxylase in rat heart and kidney. 184 10

Chronic continuous infusion of norepinephrine in rats causes alterations in biochemical and physiologic responses of the cardiovascular system and in cardiovascular adrenoceptor number. The response of cardiac and aortic ornithine decarboxylase (ODC) activity to stimulation by norepinephrine was decreased in rats receiving norepinephrine infusion. These responses are due to stimulation of beta- and alpha-adrenergic receptors, respectively. Additionally, there was reduced stimulation of aortic ODC activity by angiotensin II and vasopressin. The cardiac ODC response to angiotensin II was decreased, but the response to vasopressin was not affected. The decreased ODC response is accompanied by decreased pressor responses to the alpha-adrenergic agonist phenylephrine. Decreased numbers of alpha- and beta-adrenoceptor binding sites (as measured by the binding of [3H]prazosin and [125I]pindolol) might mediate, in part, the altered responses to adrenergic agonists. The decreased cardiovascular responsiveness measured in these animals after several days of norepinephrine infusion hypertension contrasts with the increased responses found in most other forms of hypertension. This provides a useful model in which to examine the consequences of prolonged adrenergic receptor stimulation.
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PMID:Alterations in cardiovascular responsiveness and adrenoceptor binding during catecholamine infusion hypertension in rats. 185 May 25

The onset of sympathetic innervation has been shown to play a role in the development of postsynaptic reactivity to stimulation. In the current study, we examined whether this relationship extends to responses evoked by hormonal stimuli. Rats denervated at birth by 6-hydroxydopamine treatment showed an impaired ability of vasopressin or angiotensin to stimulate cardiac ornithine decarboxylase activity. In the kidney, responsiveness was affected only for vasopressin and in the lung denervation had only transient effects on the hormonal responses. These results confirm that sympathetic input is required for proper development of some, but not all hormonal responses; the tissue specificity suggests a role of neural factors selective for cardiac development.
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PMID:Neonatal sympathectomy compromises development of responses of ornithine decarboxylase to hormonal stimulation in peripheral tissues. 263 59

Renal sympathetic function develops over the first 3 weeks of postnatal life in the rat. In the current study, the effects of neonatal sympathectomy with 6-hydroxydopamine were examined on renal biochemical and functional development. The completeness and persistence of sympathetic nerve loss were confirmed by direct measurement of norepinephrine levels and turnover. Evidence was obtained for adverse effects on cellular maturation, as shown by perturbations in the ornithine decarboxylase/polyamine system, which is controlled partially by beta adrenergic input and which regulates macromolecule synthesis in developing cells. A later phase of 6-hydroxydopamine-induced alterations in renal development was seen during the period in which synaptogenesis is prominent and sympathetic tone is high (end of the 2nd postnatal week to end of the 3rd week): the denervated kidneys displayed supersensitivity of beta adrenergically mediated cyclic AMP responses without changes in receptor binding. The alterations in biochemical indices of cellular maturation were accompanied by abnormalities of renal function. 6-Hydroxydopamine caused an increase in the fractional excretion of sodium and deficits in physiological responsiveness of the kidney to a vasopressin analog. Later on, alterations in glomerular filtration rate and basal urinary osmolality also were prominent. These results indicate that neonatal sympathectomy has an adverse effect on the biochemical and functional development of the kidney.
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PMID:Role of sympathetic neurons in biochemical and functional development of the kidney: neonatal sympathectomy with 6-hydroxydopamine. 284 47

Short-term food deprivation (FD) of preweanling rat pups causes a marked and specific suppression of liver ornithine decarboxylase (ODC) induction by alpha and beta adrenergic agonists that is mediated by postreceptor mechanisms. In the present study, we demonstrate that FD also affects the ability of adrenergic agonists to induce hepatic ODC in older animals and that these changes differ from those occurring in neonates in the duration of FD associated with changes, the subcellular mechanisms involved and the organ specificity of the effect. FD (48 hr) of 30-day-old rats caused a specific suppression of liver ODC induction by the alpha agonist phenylephrine whereas the effect of the beta agonist isoproterenol was not changed. ODC induction by vasopressin or angiotensin was unaffected, whereas the effect of aminophylline was potentiated. FD of 30-day-old rats caused a marked suppression of both alpha and beta agonist action in the heart. FD of mature (60-day-old) rats was associated with an enhanced hepatic ODC response to phenylephrine and isoproterenol. Whereas the number of receptors in heart assessed by the binding of [3H]prazosin and [125I]pindolol to alpha and beta receptors, respectively, decreased in parallel with changes in responsivity, liver ODC responses did not correlate well with receptor changes. These findings support previous findings of altered sympathetic responsivity in heart, liver and fat during FD and indicate that the sympathetic nervous system responds to FD with a complex series of changes in both pre- and postsynaptic mechanisms.
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PMID:Ontogeny of food deprivation effects on ornithine decarboxylase: ornithine decarboxylase induction by alpha and beta agonists. 286 50

Ornithine decarboxylase activity of rat lung was induced by s.c. injection of acetylcholine, norepinephrine, epinephrine, dopamine, serotonin, vasopressin, angiotensin II, and adrenocorticotropic hormone, but not by gonadotropin, aldosterone, corticosterone or hydrocortisone. The possible significance of hormonal factors in lung carcinogenesis is discussed, based on the reported promoting activity of vasopressin in cultured cells.
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PMID:Induction of ornithine decarboxylase activity in rat lung by neurotransmitters and peptide hormones. 289 98

The effects of prenatal exposure to methylmercury on the functional development of renal and hepatic response systems was examined in the developing rat. Methylmercury produced an elevation of basal activity of renal ornithine decarboxylase (ODC, an enzyme involved in regulation of cellular maturation) and an eventual relative hypertrophy; liver ODC was reduced and hypertrophy was not evident. In contrast, the reactivity of liver ODC to trophic stimulants (vasopressin, isoproterenol) was markedly enhanced by prenatal methylmercury exposure, whereas renal ODC responses were much less affected (vasopressin) or actually reduced (isoproterenol). Targeted actions of methylmercury on renal excretory function were also prominent, with increased fractional excretions of urea and electrolytes and an eventual reduction in glomerular filtration as assessed by creatinine clearance. In addition, the reactivity of the kidney to challenge with desmopressin was altered coincidentally with the appearance of the effects on basal clearance mechanisms. These studies show that doses of methylmercury ordinarily associated with selective actions on development of neurobehavioral patterns also influence the functional ontogeny of other organ systems; furthermore, the fact that the target tissues are different for prenatal vs. postnatal methylmercury exposure, indicates that the functional teratology of methylmercury exhibits critical periods of sensitivity.
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PMID:Functional consequences of prenatal methylmercury exposure: effects on renal and hepatic responses to trophic stimuli and on renal excretory mechanisms. 379 82


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